Anaphylactic or anaphylactoid reactions (treatment adjunct)—Dexamethasone (sodium phosphate injection {111}5); hydrocortisone (sodium succinate for injection {111}4); and methylprednisolone (sodium succinate for injection {111}3) are indicated as adjunctive treatment in prolonged reactions (those not responding to other forms of treatment within 1 hour), reactions requiring cardiovascular or respiratory resuscitation, or situations in which there is a significant risk of relapse.
—Epinephrine is the drug of choice for this indication. {111}2{111}1

Angioedema (treatment adjunct)—Betamethasone (tablets {111}0) is indicated as an adjunct in the treatment of angioedema. Treatment should be initiated with intramuscular or intravenous administration of a rapid-acting preparation.

[Connective tissue disease, mixed (treatment)]1
[Polyarteritis nodosa (treatment) ]1
[Polychondritis, relapsing (treatment) ]1 and
[Vasculitis (treatment)]1—Betamethasone; cortisone; dexamethasone; hydrocortisone; methylprednisolone; prednisolone; prednisone; and triamcinolone.
[Depression, mental, endogenous (diagnosis) ]1—Dexamethasone is indicated to diagnose endogenous depression and to evaluate the efficacy of treatment. Dexamethasone reduces plasma cortisol to a greater extent in control subjects than in hospitalized patients with diagnosed depression; values return toward those of control subjects as the patient responds to therapy. However, the dexamethasone suppression test is less sensitive in patients with mild to moderate depression. Also, many medications, medical problems, and other psychiatric disorders have been reported to interfere with the test results. The Health and Public Policy Committee of the American College of Physicians recommends that the dexamethasone suppression test not be used as a screening test for depression.

[Fibrositis (treatment)] and
[Myositis (treatment)]—Betamethasone (sodium phosphate and acetate injectable suspension {17}1) and dexamethasone (sodium phosphate injection {17}0).
[Nausea and vomiting, cancer chemotherapy–induced (prophylaxis)]—Dexamethasone (sodium phosphate injection, {62}9 tablets {62}8); [ hydrocortisone]1; and [ prednisone]1 are indicated to prevent nausea and vomiting induced by antineoplastic agents. The medication is administered prior to and following each course of chemotherapy. However, the advisability of administering a potent glucocorticoid to a cancer patient, unless indicated for palliation of the disease, has been questioned. Although an increased incidence of infection has not been reported in patients receiving such therapy, the possibility must be considered.
—The combination of dexamethasone plus ondansetron has been shown to provide better emetic control over cisplatin-induced emesis than ondansetron alone. {62}7{62}6{62}5{62}4

[Myasthenia gravis (treatment)]1—Betamethasone; cortisone; dexamethasone; hydrocortisone; methylprednisolone; prednisolone; prednisone; and triamcinolone are indicated for treatment of severe cases not controlled by antimyasthenic agents alone. Glucocorticoid therapy may be more effective following thymectomy and in patients having disease onset after 40 years of age. Long-term therapy may be required.

Neurotrauma
Edema, cerebral, especially when associated with primary or metastatic brain tumor, craniotomy, or head injury ( [prophylaxis ]1 and treatment)Dexamethasone (elixir, oral solution, {62}1 sodium phosphate injection, {62}0{62}9 tablets {62}8{62}7{62}6); methylprednisolone (sodium succinate for injection {62}5); and [prednisone ]1 are indicated to prevent neurosurgery-associated cerebral edema and to treat edema caused by glioblastomas or metastatic brain tumors. These medications may be less effective in treating edema caused by astrocytomas or meningiomas. Efficacy in closed head injury or ischemic brain edema has not been established. Because very high doses are required, only those glucocorticoids having little or no mineralocorticoid activity should be used.
[Ischemia, cerebral (treatment)]1—Dexamethasone.

[Spinal cord injury, acute (treatment)]—Methylprednisolone (sodium succinate for injection {62}4) is indicated in the treatment of spinal cord injury. A large study concluded that patients receiving high-dose methylprednisolone therapy within 8 hours of acute spinal cord injury recover more motor and sensory function, as compared with those receiving naloxone or placebo. {62}3{62}2 However, methylprednisolone did not improve patient prognosis when it was administered more than 8 hours after the spinal cord injury. {62}1{62}0

[Pneumonia, Pneumocystis carinii, associated with acquired immunodeficiency syndrome (AIDS) (treatment adjunct)]1—In a small number of studies, early use of corticosterioids (e.g., corticosteroid therapy begun within 24 to 72 hours of initial antipneumocystis therapy) as an adjunct to specific antipneumocystis therapy was shown to significantly reduce the risk of oxygenation deterioration, respiratory failure, and death in patients being treated for moderate-to-severe AIDS-associated pneumocystis pneumonia. {21}1{21}0{21}9{21}8{21}7{21}6{21}5{21}4 The corticosteroids used in these studies were prednisone and intravenous methylprednisolone. {21}3{21}2{21}1{21}0 No improvement in clinical outcome was shown in another study when adjunctive corticosteroid therapy was begun after the onset of respiratory failure and after the initiation of primary pneumocystis therapy. {57}9{57}8{57}7{57}6 Therefore if adjunctive corticosteroid is used, it should be started at the initiation of primary therapy for pneumocystis pneumonia in adults and children older than 13 years of age who have documented or suspected human immunodeficiency virus (HIV) infection and documented or suspected pneumocystis pneumonia, accompanied by moderate-to-severe pulmonary dysfunction (PaO 2 < 70 mm Hg on room air or A-a gradient > 35 mm Hg). {57}5{57}4{57}3 The diagnosis of HIV infection and pneumocystis pneumonia should be confirmed as soon as possible. {57}2{57}1{57}0{57}9{57}8

[Respiratory distress syndrome, adult (treatment)]1—Dexamethasone is indicated in the treatment of respiratory distress syndrome in adults, especially those with post-traumatic pulmonary insufficiency or burns, and during or following massive blood transfusions. However, the benefit of such treatment has not been established.

[Respiratory distress syndrome, neonatal (prophylaxis) ]—Betamethasone1; dexamethasone (sodium phosphate injection {57}7); and hydrocortisone1 are indicated to reduce the incidence and severity of respiratory distress syndrome (hyaline membrane disease) in premature neonates. The medication is administered to the pregnant woman, preferably 24 to 48 hours prior to delivery, to allow time for it to produce an effect. Corticosteroids are not effective when delivery is imminent. If necessary, ritodrine may be administered to delay delivery. If delivery does not occur within several days to 1 week following corticosteroid administration, but the risk of premature delivery persists, administration of a second course of corticosteroid therapy may be necessary. Corticosteroids are not effective in the treatment of respiratory distress syndrome in the premature neonate.

[Rheumatic fever (treatment)]—Betamethasone1; cortisone 1; dexamethasone1; hydrocortisone1; methylprednisolone (sodium succinate for injection {62}8); prednisolone1; prednisone1; and triamcinolone (tablets {62}7) are indicated in the treatment of rheumatic fever, especially if carditis is present.
Shock (treatment)—Betamethasone (sodium phosphate and acetate injectable suspension {62}6); cortisone (acetate injectable suspension, {62}5{62}4 tablets {62}3); dexamethasone (sodium phosphate injection {62}2{62}1); hydrocortisone (sodium phosphate injection, {62}0 sodium succinate for injection {62}9); and methylprednisolone (sodium succinate for injection {62}8{62}7{62}6) are indicated in the treatment of shock caused by adrenocortical insufficiency (Addisonian shock).
—Corticosteroids also are indicated as adjuncts in the treatment of shock associated with anaphylactic or anaphylactoid reactions. Treatment should be initiated with intramuscular or intravenous administration of a rapid-acting preparation.
—[Intravenous corticosteroids are being used as adjuncts in the treatment of septic shock. Such use is very controversial because efficacy has not been established and superimposition of new infections has been reported. Specifically, methylprednisolone has been shown to be ineffective and hazardous in the treatment of septic shock and is not recommended.]

[Transplant rejection, organ (prophylaxis and treatment) ]—Betamethasone1; cortisone1; dexamethasone1; hydrocortisone1; methylprednisolone (sodium succinate for injection, {62}5 tablets {62}4); prednisolone1; prednisone1; and triamcinolone1 are indicated concurrently with other immunosuppressants such as azathioprine or cyclosporine to reduce the risk of rejection of transplanted organs.
—[High doses of rapidly acting corticosteroids are indicated in the treatment of rejection reactions.]1

Tumors, cystic, of an aponeurosis or tendon (ganglia) (treatment) —Dexamethasone (acetate injectable suspension, {46}1 sodium phosphate injection {46}0{47}9); hydrocortisone (acetate injectable suspension {47}8); and methylprednisolone (acetate injectable suspension {47}7).Acceptance not established
There is currently not enough medical literature or clinical experience to recommend the use of prednisone for the treatment of edema associated with brain cancer.{47}6

* Approximate; applies to oral or intravenous administration only.† Anti-inflammatory, immunosuppressant, metabolic effects.‡ Sodium and water retention, potassium depletion.§ Hydrocortisone binds to transcortin (corticosteroid-binding globulin [CBG]) and to albumin. Prednisone, but not betamethasone, dexamethasone, or triamcinolone, also binds to CBG.# Although these glucocorticoids are considered not to have significant mineralocorticoid activity, hypokalemia and/or sodium and fluid retention may occur, depending on dosage and patient predisposition.Physicochemical characteristics:Molecular weight—

Corticosteroids diffuse across cell membranes and complex with specific cytoplasmic receptors. These complexes then enter the cell nucleus, bind to DNA, and stimulate transcription of messenger RNA (mRNA) and subsequent protein synthesis of various enzymes thought to be ultimately responsible for two categories of effects of systemic corticosteroids. However, these agents may suppress transcription of mRNA in some cells (e.g., lymphocytes).

For glucocorticoid effects:

Anti-inflammatory (steroidal)—Glucocorticoids decrease or prevent tissue responses to inflammatory processes, thereby reducing development of symptoms of inflammation without affecting the underlying cause. Glucocorticoids inhibit accumulation of inflammatory cells, including macrophages and leukocytes, at sites of inflammation. They also inhibit phagocytosis, lysosomal enzyme release, and synthesis and/or release of several chemical mediators of inflammation. Although the exact mechanisms are not completely understood, actions that may contribute significantly to these effects include blockade of the action of macrophage inhibitory factor (MIF), leading to inhibition of macrophage localization; reduction of dilatation and permeability of inflamed capillaries and reduction of leukocyte adherence to the capillary endothelium, leading to inhibition of both leukocyte migration and edema formation; and increased synthesis of lipomodulin (macrocortin), an inhibitor of phospholipase A2–mediated arachidonic acid release from membrane phospholipids, with subsequent inhibition of the synthesis of arachidonic acid–derived mediators of inflammation (prostaglandins, thromboxanes, and leukotrienes). Immunosuppressant actions also may contribute significantly to the anti-inflammatory effect.

Immunosuppressant—Mechanisms of immunosuppressant action are not completely understood but may involve prevention or suppression of cell-mediated (delayed hypersensitivity) immune reactions as well as more specific actions affecting the immune response. {48}0 Glucocorticoids reduce the concentration of thymus-dependent lymphocytes (T-lymphocytes), monocytes, and eosinophils. They also decrease binding of immunoglobulin to cell surface receptors and inhibit the synthesis and/or release of interleukins, thereby decreasing T-lymphocyte blastogenesis and reducing expansion of the primary immune response. Glucocorticoids also may decrease passage of immune complexes through basement membranes and decrease concentrations of complement components and immunoglobulins.

For mineralocorticoid effects:

Water and electrolyte balance: Sodium reabsorption, and potassium and hydrogen excretion, along with subsequent water retention, are mediated through an action of mineralocorticoids on the area of the renal distal tubule that facilitates sodium transport. Cation transport in other secretory cells is similarly affected. Excretion of water and electrolytes by the large intestine and by salivary and sweat glands also is altered, but to a lesser extent. Only cortisone and hydrocortisone have clinically useful mineralocorticoid activity.

Respiratory distress syndrome prophylaxis: Glucocorticoids may induce enzymes that accelerate or increase production of lung surfactant by type 2 pneumonocytes.

Other actions/effects:

Pharmacologic (supraphysiologic) doses of exogenous corticosteroids produce hypothalamic-pituitary-adrenal (HPA) axis suppression via a negative feedback mechanism, i.e., they inhibit pituitary ACTH secretion, thereby reducing ACTH-mediated production of corticosteroids and androgens in the adrenal cortex. The development of adrenocortical insufficiency and the time required for recovery of adrenal function depend primarily on the duration of corticosteroid therapy and, to a lesser extent, on dosage, timing, and frequency of administration, as well as on the potency and biologic (tissue) half-life of the specific agent. Adrenal insufficiency may occur in approximately 5 to 7 days with daily administration of doses equivalent to 20 to 30 mg of prednisone or in up to 30 days with lower doses. Following discontinuation of short-term (up to 5 days) high-dose use, adrenal recovery may occur within 1 week. Following prolonged high-dose use, complete recovery of adrenal function may require up to 1 year and, in some patients, may never occur.

Glucocorticoids stimulate protein catabolism and induce enzymes responsible for metabolism of amino acids. They decrease synthesis and increase degradation of protein in lymphoid tissue, connective tissue, muscle, and skin. With prolonged use, atrophy of these tissues may occur.

Glucocorticoids decrease bone formation and increase bone resorption. They reduce plasma calcium concentration, leading to secondary hyperparathyroidism and subsequent stimulation of osteoclasts, and directly inhibit osteoblasts. These actions, together with a decrease in the protein matrix of bone secondary to increased protein catabolism, may lead to inhibition of bone growth in children and adolescents and the development of osteoporosis at any age.Absorption:

Primarily hepatic (rapid); also renal and tissue; mostly to inactive metabolites. Cortisone and prednisone are inactive until metabolized to the active metabolites hydrocortisone and prednisolone, respectively. Fluorinated corticosteroids are metabolized more slowly than other members of the group.Duration of action:

Duration of action depends upon the route/site of administration, solubility of the dosage form, dose administered, and the condition being treated. Following oral or intravenous administration, the duration of action depends upon the biological (tissue) half-life. Following intramuscular administration, the duration of action depends upon the solubility of the dosage form as well as the biological (tissue) half-life. Following local injections, the duration of action depends upon the solubility of the dosage form and the specific route/site of administration.Elimination:
Primarily by renal excretion of inactive metabolites.

Precautions to ConsiderPregnancy/Reproduction
Fertility—
Corticosteroids have been reported to increase or decrease the number or motility of spermatozoa. {68}9{68}8{68}7{68}6{68}5{68}4{68}3 However, it is not known whether reproductive capacity in humans is adversely affected.

Pregnancy—

For corticosteroids

Corticosteroids cross the placenta. {68}2{68}1{68}0{70}9 Although adequate studies have not been done in humans, there is some evidence that pharmacologic doses of corticosteroids may increase the risk of placental insufficiency, decreased birthweight, or stillbirth. However, teratogenic effects in humans have not been confirmed.

Prenatal administration of betamethasone or dexamethasone to the pregnant woman to prevent respiratory distress syndrome in the premature neonate has not been shown to affect the child's growth or development adversely. Physiologic replacement doses of corticosteroids administered for treatment of maternal adrenal insufficiency also are unlikely to adversely affect the fetus or neonate.

High doses of budesonide administered subcutaneously produced fetal malformations (primarily skeletal defects) in rabbits, rats, and mice. However, the relevance of these findings to humans has not been established. {70}5

Breast-feeding

For corticosteroids—Problems in humans have not been documented. Administration of physiologic doses or low pharmacologic doses (the equivalent or less of 25 mg of cortisone or 5 mg of prednisone per day) is not considered likely to affect the infant adversely. Less than 1% of the administered dose of prednisolone is distributed into breast milk. {70}4 However, breast-feeding during the use of higher pharmacologic doses is not recommended because corticosteroids are distributed into breast milk {70}3{70}2{70}1{70}0{71}9{71}8{71}7{71}6{71}5{71}4{71}3 and may cause unwanted effects, such as growth suppression and inhibition of endogenous steroid production, in the infant. {71}2{71}1{71}0{77}9{77}8{77}7Pediatrics

Chronic use of corticosteroids may suppress growth and development of the pediatric or adolescent patient and should be undertaken with caution. {57}4{57}3 Use of long-acting glucocorticoids (betamethasone and dexamethasone) or daily doses of any corticosteroid that are larger than replacement therapy doses are especially likely to inhibit growth and are not recommended for any form of chronic therapy. For long-term therapy, a short-acting agent (cortisone or hydrocortisone) or an intermediate-acting agent (methylprednisolone, prednisolone, prednisone, or triamcinolone) is recommended. Alternate-day therapy with an oral intermediate-acting corticosteroid may decrease growth retardation effects. {57}2{57}1 Some clinicians recommend that only cortisone, hydrocortisone, or prednisone be used for long-term replacement therapy. Also, pediatric patients may be at increased risk of developing osteoporosis, avascular necrosis of the femoral heads, glaucoma, or cataracts during prolonged therapy. Children and adolescents receiving prolonged therapy should be closely monitored.

Pediatric dosage is determined more by the severity of the condition and the response of the patient than by age or body weight. {57}0 Also, for treatment of adrenocortical insufficiency, pediatric dosage is preferably determined in terms of mg per square meter of body surface area. Determination of pediatric dosage in terms of mg per kg of body weight (mg/kg) increases the possibility of overdosage, especially in very young, short, or heavy children.

Geriatrics

Geriatric patients may be more likely to develop hypertension during corticosteroid therapy. {62}9 Geriatric patients, especially postmenopausal women, also may be more likely to develop glucocorticoid-induced osteoporosis.Drug interactions and/or related problems
The following drug interactions and/or related problems have been selected on the basis of their potential clinical significance (possible mechanism in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):

Note: Combinations containing any of the following medications, depending on the amount present, also may interact with this medication.
Interactions listed below involving alterations in serum potassium concentration and/or changes in sodium or fluid balance are especially likely to occur with corticosteroids having significant mineralocorticoid activity. However, these interactions also may occur with other corticosteroids, depending on dosage and patient predisposition.

Acetaminophen (induction of hepatic enzymes by corticosteroids may increase the formation of a hepatotoxic acetaminophen metabolite, thereby increasing the risk of hepatotoxicity, when they are used concurrently with chronic or high-dose acetaminophen therapy)

Alcohol or
Anti-inflammatory drugs, nonsteroidal (NSAIDs) (risk of gastrointestinal ulceration or hemorrhage may be increased when these substances are used concurrently with glucocorticoids; however, concurrent use of NSAIDs in the treatment of arthritis may provide additive therapeutic benefit and permit glucocorticoid dosage reduction)

» Aminoglutethimide (aminoglutethimide suppresses adrenal function so that glucocorticoid supplementation may be required; however, aminoglutethimide accelerates the metabolism of dexamethasone so that the half-life of dexamethasone may be reduced twofold; hydrocortisone is recommended instead because its metabolism is not known to be altered by aminoglutethimide and because its mineralocorticoid activity also may be required)

» Amphotericin B, parenteral {62}8{62}7 or
Carbonic anhydrase inhibitors (concurrent use with corticosteroids may result in severe hypokalemia and should be undertaken with caution; {62}6 serum potassium concentrations and cardiac function should be monitored during concurrent use)

(the use of hydrocortisone to control adverse reactions to amphotericin B has resulted in cases of cardiac enlargement and congestive heart failure {62}5{62}4)

(concurrent use of corticosteroids with acetazolamide sodium may increase the risk of hypernatremia and/or edema because corticosteroids cause sodium and fluid retention; the risk with corticosteroids may depend on the patient's sodium requirement as determined by the condition being treated)

(the possibility should be considered that concurrent chronic use of both carbonic anhydrase inhibitors and corticosteroids may increase the risk of hypocalcemia and osteoporosis because carbonic anhydrase inhibitors also increase calcium excretion)

Anabolic steroids or
Androgens (concurrent use with glucocorticoids may increase the risk of edema; also, concurrent use may promote the development of severe acne)

» Antacids (concurrent chronic use with prednisone or dexamethasone may decrease absorption of these glucocorticoids; efficacy may be decreased sufficiently to require dosage adjustment in patients receiving small doses, but probably not in those receiving large doses, of the corticosteroid)

(the potential occurrence of gastrointestinal ulceration or hemorrhage during glucocorticoid therapy, and the effects of glucocorticoids on vascular integrity, may cause increased risk to patients receiving anticoagulant or thrombolytic therapy)

Antidepressants, {62}2 tricyclic (these medications do not relieve, and may exacerbate, corticosteroid-induced mental disturbances; they should not be used for treatment of these adverse effects {62}1)

Antithyroid agents or
Thyroid hormones {62}6 (changes in the thyroid status of the patient that may occur as a result of administration, changes in dosage, or discontinuation of thyroid hormones or antithyroid agents may necessitate adjustment of corticosteroid dosage because metabolic clearance of corticosteroids is decreased in hypothyroid patients and increased in hyperthyroid patients; {62}5 dosage adjustment should be based on results of thyroid function tests {62}4)

Asparaginase (glucocorticoids, especially prednisone, may increase the hyperglycemic effect of asparaginase and the risk of neuropathy and disturbances in erythropoiesis; the toxicity appears to be less pronounced when asparaginase is administered following, rather than before or with, these medications)

Contraceptives, oral, estrogen-containing {62}3 or
Estrogens {62}2{62}1 (estrogens may alter the metabolism and protein binding of glucocorticoids, leading to decreased clearance, increased elimination half-life, and increased therapeutic and toxic effects of the glucocorticoid; glucocorticoid dosage adjustment may be required during and following concurrent use {62}0)

» Digitalis glycosides {62}1{62}0 (concurrent use with glucocorticoids may increase the possibility of arrhythmias or digitalis toxicity {62}9{62}8 associated with hypokalemia)

» Diuretics {62}7{62}6{62}5{62}4{62}3{62}2 (natriuretic and diuretic effects of these medications may be decreased by sodium- and fluid-retaining actions of corticosteroids, and vice versa )

(concurrent use of potassium-depleting diuretics with corticosteroids may result in severe hypokalemia; {62}1{62}0{62}9{62}8{62}7{62}6 monitoring of serum potassium concentration and cardiac function is recommended )

(effects of potassium-sparing diuretics and/or corticosteroids on serum potassium concentration may be decreased during concurrent use; monitoring of serum potassium concentration is recommended)

Immunosuppressant agents, other (concurrent use with immunosuppressant doses of glucocorticoids may increase the risk of infection and possibly the development of lymphomas or other lymphoproliferative disorders; these neoplasms may be associated with Epstein-Barr virus infections; a few studies in organ transplant patients receiving immunosuppressant therapy indicate that progression of the neoplasm may be reversed after immunosuppressant dosage is decreased or therapy is discontinued)

Iophendylate or
Metrizamide (concurrent intrathecal administration of metrizamide or iophendylate with intrathecal administration of glucocorticoids may increase the risk of arachnoiditis )

Isoniazid {62}2{62}1 (glucocorticoids, especially prednisolone, may increase hepatic metabolism and/or excretion of isoniazid, leading to decreased plasma concentration and effectiveness of isoniazid, {62}0{48}9 especially in patients who are rapid acetylators; isoniazid dosage adjustment may be required during and following concurrent use)

Mexiletine (concurrent use with glucocorticoids may accelerate metabolism of mexiletine, leading to decreased mexiletine plasma concentration)

» Mitotane (mitotane suppresses adrenocortical function; glucocorticoid supplementation usually is required during mitotane administration, but higher doses than those generally used for replacement therapy may be required because mitotane alters glucocorticoid metabolism)

Neuromuscular blocking agents, nondepolarizing (hypokalemia induced by glucocorticoids may enhance the blockade of nondepolarizing neuromuscular blocking agents, possibly leading to increased or prolonged respiratory depression or paralysis [apnea]; serum potassium determinations may be necessary prior to administration of these agents)

(hydrocortisone and prednisone also have been reported to decrease the efficacy of pancuronium by an unknown mechanism; increased dosage of pancuronium or use of an alternate neuromuscular blocking agent may be necessary)

» Potassium supplements (effects of these medications and/or corticosteroids on serum potassium concentration may be decreased when these medications are used concurrently; monitoring of serum potassium concentration is recommended)

» Ritodrine (concurrent use may cause pulmonary edema in the pregnant woman; maternal death has been reported; both medications should be discontinued at the first sign of pulmonary edema)

Salicylates {48}8{48}7{48}6{48}5{48}4{48}3{48}2{48}1{48}0{62}9{62}8{62}7{62}6{62}5{62}4 (although concurrent use with glucocorticoids in the treatment of arthritis may provide additive therapeutic benefit and permit glucocorticoid dosage reduction, glucocorticoids may increase salicylate excretion and reduce salicylate plasma concentrations so that the salicylate dosage requirement may be increased; {62}3{62}2{62}1{62}0{62}9 salicylism may occur when glucocorticoid dosage is subsequently decreased or discontinued, especially in patients receiving large [antirheumatic] doses of salicylates; {62}8{62}7{62}6{62}5{62}4 also, the risk of gastrointestinal ulceration or hemorrhage may be increased during concurrent use)

» Sodium-containing medications or foods (concurrent use with pharmacologic doses of glucocorticoids may result in edema and increased blood pressure, possibly to hypertensive levels)

(although patients receiving replacement doses of glucocorticoids may require sodium supplementation, adjustment of dietary sodium intake may be required when a medication having a high sodium content is administered concurrently )

(It is recommended that these doses not be exceeded during somatrem or somatropin therapy; if larger doses are required, administration of somatrem or somatropin should be postponed)

Streptozocin (concurrent use with glucocorticoids may increase the risk of hyperglycemia )

Troleandomycin {48}0{62}9{62}8{62}7 (troleandomycin may decrease metabolism of methylprednisolone and possibly other glucocorticoids, leading to increased plasma concentration, elimination half-life, and therapeutic and toxic effects; {62}6{62}5{62}4{62}3 glucocorticoid dosage adjustment may be required during and following concurrent use {62}2{62}1{62}0{85}9)

» Vaccines, live virus, or other immunizations {85}8{85}7{85}6{85}5{85}4{85}3{85}2{85}1{85}0{86}9{86}8{86}7{86}6{86}5{86}4 (administration of live virus vaccines to patients receiving pharmacologic [immunosuppressant] doses of glucocorticoids may potentiate replication of the vaccine virus, thereby increasing the risk of the patient's developing the viral disease, and/or decreasing the patient's antibody response to the vaccine and is not recommended; {86}3{86}2 the patient's immunologic status should be evaluated prior to administration of a live virus vaccine; also, immunization with oral poliovirus vaccine should be postponed in persons in close contact with the patient, especially family members)

(other immunizations are not recommended in patients receiving pharmacologic [immunosuppressant] doses of glucocorticoids because of the increased risk of neurological complications and the possibility of decreased or absent antibody response {86}1{86}0{85}9{85}8{85}7{85}6)

(immunizations may be administered to patients receiving glucocorticoids via routes or in quantities that are not likely to cause immunosuppression, for example, those receiving local injections, short-term [less than 2 weeks] therapy, or physiologic doses {85}5{85}4{85}3{85}2{85}1)

Laboratory value alterations
The following have been selected on the basis of their potential clinical significance (possible effect in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):

With results of dexamethasone suppression tests

Due to other medications
Alcohol (chronic abuse) or
Glutethimide or
Meprobamate or
Methaqualone or
Methyprylon (may cause false-positive results in test for endogenous depression)

Due to medical problems or conditions
Adrenal hyperfunction (Cushing's disease) or
Anorexia nervosa or malnutrition leading to extreme weight loss, recent or
Carcinoma, disseminated, with concurrent serious infection or
Cardiac failure or
Dehydration or
Diabetes mellitus, unstable or
Fever or
Hypertension or
Pregnancy or
Renal failure or
Temporal lobe disease (may cause false-positive results in test for endogenous depression)

With other diagnostic test results
Brain imaging using sodium pertechnetate Tc 99m, technetium Tc 99m gluceptate, or technetium Tc 99m pentetate (uptake of these diagnostic aids into cerebral tumors may be decreased in patients receiving large doses of glucocorticoids because of glucocorticoid-induced reduction of peritumor edema)

Gonadorelin test for hypothalamic-pituitary-gonadal axis function (glucocorticoids may alter the results of the gonadorelin test by affecting pituitary secretion of gonadotropins through a complicated feedback mechanism )

Protirelin test for thyroid function (physiologic doses of corticosteroids have no effect, but pharmacologic doses may reduce the thyroid-stimulating hormone [TSH] response to protirelin; however, withdrawal of corticosteroids in patients with known hypopituitarism is generally not recommended)

Uric acid, serum (concentrations may be increased in patients with acute leukemia but may be decreased in other patients because of weak uricosuric effect)

White blood count (may be decreased)

Medical considerations/Contraindications
The medical considerations/contraindications included have been selected on the basis of their potential clinical significance (reasons given in parentheses where appropriate)— not necessarily inclusive (» = major clinical significance).

» Placental insufficiency» Premature membrane rupture (increased risk of maternal infection; the glucocorticoid should be administered immediately if this occurs, since the risk of infection increases with time )

Risk-benefit should be considered when the following medical problems exist

For all indications:» Acquired immunodeficiency syndrome (AIDS) or {49}6» Human immunodeficiency virus (HIV) infection {49}5{49}4 (although pharmacologic doses of corticosteroids can be effective in the treatment of certain HIV-related diseases, careful medical evaluation of the risks and benefits of this therapy must be done, due to the possible increased risk of severe uncontrollable infections and/or neoplasms; {49}3{49}2{49}1 in one study in patients given tapering doses of intravenous methylprednisolone starting with 60 mg every 6 hours for 8 days as an adjunct to antipneumocystis therapy, an increase in frequency or severity of life-threatening opportunistic infections was observed; {49}0{49}9{49}8 in a study of similar patients given tapering doses of prednisone starting at 40 mg two times a day for 21 days, no increase in the incidence of Kaposi's sarcoma or life-threatening opportunistic infections was observed, though the incidence of oral candidiasis and mucocutaneous herpes simplex infection did increase {49}7{49}6{49}5)

Hepatic function impairment or disease {51}4 (increased risk of glucocorticoid toxicity, especially if hypoalbuminemia is present; possibility of impaired conversion of cortisone or prednisone to their active metabolites, although this effect may be offset by decreased protein binding or clearance and/or conversion in other tissues)

Herpetic lesions, oral
Hyperlipidemia (concentrations of fatty acids or cholesterol may be increased)

Hypersensitivity to corticosteroids {23}3{23}2{23}1{23}0{62}9
Hyperthyroidism {62}8 (glucocorticoid effect may be impaired because of accelerated metabolism; this may be especially important with physiologic doses or low pharmacologic doses)

Ophthalmologic examinations (may be required at periodic intervals for adults or children receiving therapy for more than 6 weeks to detect the presence of cataracts, glaucoma, increased intraocular pressure, or ocular infections)

Note: The risk of adverse effects with pharmacologic doses of corticosteroids generally increases with the duration of therapy and frequency of administration and, to a lesser extent, with dosage.
Chronic administration of physiologic replacement doses of corticosteroids rarely causes adverse effects.
Administration of glucocorticoids via local injection reduces the risk of systemic effects. The risk of both systemic and local adverse effects is still present to a degree, however, and increases with the frequency of injections.
Pharmacologic doses of glucocorticoids lower resistance to infection; the patient may be predisposed to systemic infections during, and for a time following, therapy. Increased susceptibility to infection may occur with short-term high-dose use (“pulse” therapy) as well as with more prolonged use. Also, symptoms of onset or progression of infections may be masked.

The following side/adverse effects have been selected on the basis of their potential clinical significance (possible signs and symptoms in parentheses where appropriate)—not necessarily inclusive:Those indicating need for medical attentionIncidence less frequentDiabetes mellitus (decreased or blurred vision; frequent urination; increased thirst){52}5{52}4{52}3{52}2{52}1{52}0{62}9{62}8{62}7{62}6{62}5{62}4{62}3{62}2{62}1

Note:Psychic disturbances are more likely to occur in patients with chronic debilitating illnesses that predispose them to psychic disturbances and in patients receiving higher daily dosages. Psychic disturbances may be related to dose rather than duration of therapy; symptoms may appear within a few days to 2 weeks after initiation of therapy and usually are associated with doses equivalent to 40 mg or more of prednisone per day. Additionally, euphoria or fear of relapse may lead to psychological dependence or abuse of corticosteroids.Sudden blindness following injection into sites in the head or neck area, {62}9{62}8{62}7{62}6{62}5{62}4 such as nasal turbinates or scalp, is due to possible entry of drug crystals into ocular blood vessels.

Note: Rapid intravenous administration of high doses of corticosteroids has been reported to cause angioedema and/or anaphylactic reactions, seizures, and sudden death associated with cardiac arrhythmias. {62}4 Monitoring of the electrocardiogram (ECG) is recommended. Equipment, medications, and trained personnel necessary for treating these complications should be immediately available.

Those indicating need for medical attention only if they continue or are bothersomeIncidence more frequentGastrointestinal irritation (nausea; vomiting){06}{10}{18}{30}{33}increased appetite{04}{06}{10}{30}{33}indigestion{29}nervousness or restlessnesstrouble in sleeping{50}weight gain{10}

Note:Hypopigmentation is more likely at the injection site.Flushing of face or cheeks may persist for 24 to 48 hours.Increased joint pain may occur within a few hours postinjection and persist for up to 48 hours.

Breast-feeding—Breast-feeding is not recommended during use of higher pharmacologic doses

Use in children—Infants born to women who received corticosteroids during pregnancy should be monitored for signs of hypoadrenalism; close monitoring also is required during chronic therapy because suppression of growth and development may result; possible increased severity of chickenpox or measles in children receiving immunosuppressant doses; increased risk for developing osteoporosis, avascular necrosis of the femoral heads, glaucoma, or cataracts during prolonged therapy

* Bracketed information refers to routes of administration that are not included in U.S. product labeling.† Abbreviations: Systemic—IM = intramuscular; IV = intravenous; SC = subcutaneous. Local—IA = intra-articular; IB = intrabursal; IL = intralesional; IS = intrasynovial; ST = soft tissue; IT = intraturbinal.1 Not included in Canadian product labeling.
For replacement therapy in chronic adrenocortical insufficiency states, corticosteroid therapy must be continued for the life of the patient. It is recommended that dosage of cortisone or hydrocortisone be timed to simulate endogenous corticosteroid secretion, with two thirds of the daily dose administered in the morning and one third in the evening. Other corticosteroids usually are given once a day.

For treatment of congenital adrenal hyperplasia, suppression of corticotropin secretion is required to decrease hypersecretion of adrenal androgens. This usually is achieved by administering one third of the daily dose of cortisone or hydrocortisone in the morning and two thirds in the evening or giving one third of the daily dose three times a day at evenly spaced intervals. Other corticosteroids usually are given once a day.

Clinically significant hypothalamic-pituitary-adrenal (HPA) axis suppression leading to adrenal insufficiency may occur more readily with multiple daily doses or evening administration than with single doses given every morning or every other morning. Administration of a single daily dose of a short- or intermediate-acting corticosteroid prior to 9 a.m. may reduce the risk of HPA axis suppression (because maximum endogenous corticosteroid secretion occurs in the morning) and is recommended for daily administration whenever possible. However, some disease conditions may require multiple daily doses.

Following discontinuation of short-term (up to 5 days) high-dose use, adrenal recovery may occur within 1 week. However, following prolonged high-dose administration, complete recovery of adrenal function may require up to 1 year. Following very prolonged suppression, complete recovery may never occur. During the recovery period, monitoring of adrenal function may be required to assess the patient's ability to respond to stress.

For oral dosage forms only
If oral long-term use is required for disease therapy, an alternate-day regimen using an intermediate-acting corticosteroid is recommended to minimize HPA axis suppression and possibly other adverse effects. An intermediate-acting corticosteroid is one that suppresses HPA axis activity for 12 to 36 hours following a single dose. Administration of longer-acting corticosteroids on an alternate-day schedule does not reduce the risk of HPA axis suppression and is not recommended.

Alternate-day therapy utilizes a single dose administered every other morning, usually in a quantity equivalent to, or somewhat higher than, twice the usual or pre-established daily dose. The patient should have a normal or moderately responsive HPA axis.

If treatment has been initiated with daily administration, changes to alternate-day therapy should be made gradually, after the patient's condition has stabilized. However, for some diseases, such as childhood nephrotic syndrome, therapy may be initiated with alternate-day dosing.

Alternate-day therapy may not be effective in treating hematologic disorders, malignancies, ulcerative colitis, or severe conditions. Also, some patients, such as those with asthma or rheumatoid arthritis, may experience exacerbation of symptoms on the second day. Administration of (or increasing the dosage of) suitable supplemental therapy on the second day may provide sufficient symptomatic relief to permit alternate-day dosing in some patients.

For parenteral dosage forms only
For acute adrenocortical insufficiency, initiation of corticosteroid therapy by intravenous injection followed by slow intravenous infusion or intramuscular administration is recommended. Certain other acute conditions also may require initiation of therapy with intramuscular or intravenous administration of a rapidly acting formulation.

In severe or life-threatening conditions, single-dose or short-term intravenous administration of a very high dose (“pulse” therapy) may produce the required therapeutic response with a minimum risk of prolonged HPA axis suppression or other adverse effects. Such therapy has been recommended for treating conditions such as organ transplant rejection reactions, acute nephritis associated with systemic lupus erythematosus, vasculitis, adult respiratory distress syndrome, and shock. However, rapid intravenous administration of high doses of corticosteroids has been reported to cause potentially life-threatening side effects and appropriate precautions should be observed.

When the suspension dosage forms are administered intramuscularly, they should be injected deeply into the gluteal muscle to prevent local tissue atrophy. It is recommended that the deltoid muscle not be used because of a higher incidence of local atrophy. In addition, do not inject repeatedly into the same site.

A standard textbook should be consulted for specific techniques and procedures applicable to local injection of corticosteroids for various indications.

Following intra-articular injection, the injected joint should not be overused, even if pain is relieved, because of the increased risk of joint damage or deterioration. {26}{50} It is recommended that weight-bearing joints be rested for 24 to 48 hours postinjection.

Administration of a local anesthetic concurrently with intra-articular or soft tissue injection of a corticosteroid may reduce the pain of injection and provide immediate relief of symptoms. However, a postinjection flare of pain may occur when the local anesthetic effect subsides.

Dosages for local injections (e.g., intra-articular, intrabursal, intradermal, intralesional) are given as ranges only. The actual dosage depends upon the size of the joint or lesion and the severity of the condition being treated. {10}Diet/Nutrition
Administration of oral dosage forms with food may relieve the indigestion or mild gastrointestinal irritation that may occur. {06}

Administration of calcium and vitamin D and, if the patient's condition permits, exercise or physical therapy may reduce the risk of corticosteroid-induced osteoporosis during prolonged therapy.For treatment of adverse effectsRecommended treatment consists of the following:

• For gastrointestinal effects—Administration of antacids between meals may relieve indigestion or mild gastrointestinal irritation that may occur during parenteral, as well as oral, corticosteroid therapy. However, the efficacy of antacids or other antiulcer medications in preventing severe gastrointestinal problems, such as ulceration, hemorrhage, and/or bowel perforation, during corticosteroid therapy has not been established.
• For mental depression or psychoses—If possible, decrease corticosteroid dosage or discontinue therapy. A phenothiazine may be administered if necessary; lithium also has been recommended. Some patients may require electroconvulsive therapy if severe depression persists. Tricyclic antidepressants should not be used since they do not relieve, and may exacerbate, corticosteroid-induced mental disturbances. Prophylactic administration of an antipsychotic agent may be indicated if additional courses of corticosteroid therapy are required by a patient with a history of corticosteroid-induced psychosis.
• For withdrawal effects (non-HPA axis suppression)—Administration of aspirin or another nonsteroidal anti-inflammatory drug may alleviate some of the symptoms of this condition.

Usual pediatric dose
Adrenocortical insufficiency
Intramuscular, 0.018 mg (base) per kg of body weight or 0.5 mg per square meter of body surface area a day (in three divided doses) every third day; or 0.0058 to 0.0088 mg per kg of body weight or 0.17 to 0.25 mg per square meter of body surface area once a day.

Other indications
Intramuscular, 0.021 to 0.13 mg per kg of body weight or 0.63 to 3.75 mg per square meter of body surface area every twelve to twenty-four hours.

6 mg (3 mg of betamethasone acetate and 3 mg of betamethasone base) per mL (Rx) [Celestone Soluspan{39}]Packaging and storage:
Store between 2 and 25 °C (36 and 77 °F), protected from light, {03}{39} unless otherwise specified by manufacturer. Protect from freezing.Incompatibilities:
This medication should not be mixed with parenteral-local anesthetic formulations containing parabens, phenol, or other such preservatives, because flocculation of the corticosteroid may occur. {03} The required quantity of corticosteroid suspension should be drawn into the syringe first, then the local anesthetic added. Do not introduce the local anesthetic directly into the multiple-dose vial. {03}Auxiliary labeling:
• Shake well. {03}{39}Additional information:
For administration of injections, see manufacturer's labeling.

Usual pediatric dose
Adrenocortical insufficiency
Intramuscular, 0.7 mg per kg of body weight or 37.5 mg per square meter of body surface area a day every third day; or 0.23 to 0.35 mg per kg of body weight or 12.5 mg per square meter of body surface area once a day.

Other indications
Intramuscular, 0.83 to 5 mg per kg of body weight or 25 to 150 mg per square meter of body surface area every twelve to twenty-four hours.

50 mg per mL (Rx) [Cortone (benzyl alcohol){30}]Packaging and storage:
Store below 40 °C (104 °F), preferably between 15 and 30 °C (59 and 86 °F), unless otherwise specified by manufacturer. Protect from freezing. {04}Stability:
Dilutions or admixtures of this medication with other products are not recommended because the state of suspension or the rate of absorption may be affected.

This medication is heat-sensitive and should not be autoclaved. {04}{30}Auxiliary labeling:
• Shake well.

Caution:
Use of preparations containing benzyl alcohol is not recommended in neonates. A fatal toxic syndrome consisting of metabolic acidosis, central nervous system (CNS) depression, respiratory problems, renal failure, hypotension, and possibly seizures and intracranial hemorrhages has been associated with this use.Additional information:
Do not administer this medication intravenously.

Note: Bracketed uses in the Dosage Forms section refer to categories of use and/or indications that are not included in U.S. product labeling.DEXAMETHASONE ELIXIR USPUsual adult and adolescent dose
Corticosteroid
Oral, 0.75 to 9 mg a day as a single dose or in divided doses. {06}{07}

[Dexamethasone suppression test]1
Test for Cushing's syndrome: Oral, 1 mg as a single dose at 11:00 p.m. or 0.5 mg every six hours for forty-eight hours. {06}{07}{25}{34}

Test to distinguish Cushing's syndrome due to pituitary ACTH excess from Cushing's syndrome due to other causes: Oral, 2 mg every six hours for forty-eight hours. {06}{07}{25}{34}

Edema, cerebral, associated with recurrent or inoperable brain tumor
Oral, 2 mg two or three times a day, administered as maintenance therapy after cerebral edema has initially been controlled using parenteral dexamethasone sodium phosphate. {07}{25}{34}

Usual pediatric dose
Adrenocortical insufficiency
Oral, 0.023 mg per kg of body weight or 0.67 mg per square meter of body surface area a day in three divided doses.

Other indications
Oral, 0.083 to 0.33 mg per kg of body weight or 2.5 to 10 mg per square meter of body surface area a day in three or four divided doses.

Canada—
Not commercially available.Packaging and storage:
Store between 15 and 30 °C (59 and 86 °F), unless otherwise specified by manufacturer, in a tight container. {32} Protect from freezing.Preparation of dosage form:Dexamethasone Intensol should be mixed with water, juice, soft drink, applesauce, or pudding before administration. {25}Stability:Dexamethasone Intensol should be consumed immediately after it is mixed with a beverage or a semi-solid food. {25} Any unused portion should be discarded. {25}

Allergic disorders
Therapy should be initiated with dexamethasone sodium phosphate injection (see Dexamethasone Sodium Phosphate Injection USP). Then, beginning on the second day, oral, 3 mg in two divided doses for two days, 1.5 mg in two divided doses for one day, 0.75 mg for two days, and a follow-up visit on the eighth day. {08}{25}

[Nausea and vomiting, cancer chemotherapy–induced]
Therapy should be initiated with dexamethasone sodium phosphate injection (see Dexamethasone Sodium Phosphate Injection USP). Then, oral, 4 mg every four to six hours, or 8 mg every eight hours with the dosage being reduced gradually over two to three days. {34} Duration of therapy should not exceed five days beyond administration of chemotherapy. {34}

Canada—
Not commercially available.Packaging and storage:
Store between 15 and 30 °C (59 and 86 °F), {64} unless otherwise specified by manufacturer. Protect from freezing. {09} Protect from light. {64}Stability:
This medication is heat-sensitive and should not be autoclaved. {09}{64}Auxiliary labeling:
• Shake well. {64}Additional information:
For administration of injections, see manufacturer's labeling.

Do not administer this medication intravenously.

The suspension containing the equivalent of 16 mg of dexamethasone per mL is not for intralesional use.

DEXAMETHASONE SODIUM PHOSPHATE INJECTION USP

Note: The dosing and strength of the dosage forms available are expressed in terms of dexamethasone phosphate.

Edema, cerebral
Initial: Intravenous, 10 mg, followed by 4 mg intramuscularly every six hours until symptoms subside. {08}{33}{60} Dosage may be reduced after two to four days and gradually discontinued over a period of five to seven days, {33} unless a brain tumor, which must be treated before dexamethasone can be discontinued, is present. {08}

Maintenance (for recurrent or inoperable brain tumors): Intramuscular, 2 mg two or three times a day initially, then adjusted according to patient response. {08}{33}

Shock

The following regimens have been utilized:
Intravenous, 20 mg as a single dose initially, followed by 3 mg per kg of body weight per twenty-four hours via continuous intravenous infusion, {08}{33}{60} or

Intravenous, 2 to 6 mg per kg of body weight as a single injection, {08}{33} or

Intravenous, 40 mg as a single dose, administered every two to six hours as needed, {08}{33}{60} or

Intravenous, 1 mg per kg of body weight as a single injection. {08}{33}

Note: Administration of high-dose therapy for shock should be discontinued after the patient's condition has stabilized and usually is continued for no longer than two to three days. {08}{33}

[Nausea and vomiting, cancer chemotherapy–induced]
Intravenous, 8 to 20 mg administered over five to fifteen minutes beginning just prior to chemotherapy. Therapy should be continued with dexamethasone tablets {33} (see Dexamethasone Tablets USP).

[Respiratory distress syndrome, neonatal (prophylaxis)]
Intramuscular, 5 mg every twelve hours up to a total of four doses beginning seven days to twenty-four hours before the estimated delivery date. {33}

Usual adult prescribing limits
80 mg daily. {33}Usual pediatric dose
Adrenocortical insufficiency
Intramuscular, 0.023 mg (dexamethasone phosphate) per kg of body weight or 0.67 mg per square meter of body surface area a day (in three divided doses) every third day; or 0.0078 to 0.012 mg per kg of body weight or 0.23 to 0.34 mg per square meter of body surface area once a day.

Other indications
Intramuscular, 0.028 to 0.17 mg per kg of body weight or 0.83 to 5 mg per square meter of body surface area every twelve to twenty-four hours.

For use in cancer chemotherapy–induced nausea and vomiting, 20 mg of dexamethasone sodium phosphate injection may be admixed with 8 mg of ondansetron hydrochloride injection in 50 mL of 5% dextrose injection. {33}Stability:
This medication is heat-sensitive and should not be autoclaved. {08}{33}

When dexamethasone sodium phosphate injection is admixed with dextrose injection or sodium chloride injection, the solution must be used within 24 hours. {08}

When dexamethasone sodium phosphate injection is admixed with ondansetron hydrochloride injection in 5% dextrose injection, the resulting solution is stable for up to two days when stored at room temperature or for up to 7 days when stored at a temperature between 2 and 8 °C (36 and 46 °F). {33}

Caution:
Use of preparations containing benzyl alcohol is not recommended in neonates. A fatal toxic syndrome consisting of metabolic acidosis, central nervous system (CNS) depression, respiratory problems, renal failure, hypotension, and possibly seizures and intracranial hemorrhages has been associated with this use.Additional information:
For administration of injections, see manufacturer's labeling.

Usual pediatric dose
Adrenocortical insufficiency
Intramuscular, 0.56 mg per kg of body weight or 30 to 37.5 mg per square meter of body surface area a day every third day; or 0.19 to 0.28 mg per kg of body weight or 10 to 12.5 mg per square meter of body surface area once a day.

Other indications
Intramuscular, 0.67 to 4 mg per kg of body weight or 20 to 120 mg per square meter of body surface area every twelve to twenty-four hours.

Canada—
Not commercially available.Packaging and storage:
Store below 40 °C (104 °F), preferably between 15 and 30 °C (59 and 86 °F), unless otherwise specified by manufacturer. Protect from freezing.Stability:
For concurrent use of a parenteral-local anesthetic, withdraw the required quantity of corticosteroid suspension into a syringe, then add the local anesthetic. {10}Do not introduce the local anesthetic directly into the multiple-dose vial. Also, the mixture must be used immediately and any unused portion discarded. {10}

This medication is heat-sensitive and should not be autoclaved. {10}Auxiliary labeling:
• Shake well.

Caution:
Use of preparations containing benzyl alcohol is not recommended in neonates. A fatal toxic syndrome consisting of metabolic acidosis, central nervous system (CNS) depression, respiratory problems, renal failure, hypotension, and possibly seizures and intracranial hemorrhages has been associated with this use.Additional information:
For administration of injections, see manufacturer's labeling.

Do not administer this medication intravenously.

HYDROCORTISONE SODIUM PHOSPHATE INJECTION USP

Note: The dosing and strength of the dosage form available is expressed in terms of hydrocortisone base (not the sodium phosphate salt).

Usual pediatric dose
Adrenocortical insufficiency
Intramuscular or intravenous, 0.19 to 0.28 mg (base) per kg of body weight or 10 to 12 mg per square meter of body surface area a day in three divided doses.

Other indications
Intramuscular, 0.67 to 4 mg per kg of body weight or 20 to 120 mg per square meter of body surface area every twelve to twenty-four hours.

Canada—
Not commercially available.Packaging and storage:
Store below 40 °C (104 °F), preferably between 15 and 30 °C (59 and 86 °F), unless otherwise specified by manufacturer. Protect from freezing.Preparation of dosage form:
Hydrocortisone sodium phosphate injection may be admixed with dextrose injection or sodium chloride injection and administered via intravenous infusion. {12}Stability:
This medication is heat-sensitive and should not be autoclaved. {12}

When hydrocortisone sodium phosphate injection is admixed with dextrose injection or sodium chloride injection, the solution must be used within 24 hours. {12}

Caution:
Use of preparations containing benzyl alcohol is not recommended in neonates. A fatal toxic syndrome consisting of metabolic acidosis, central nervous system (CNS) depression, respiratory problems, renal failure, hypotension, and possibly seizures and intracranial hemorrhages has been associated with this use. {12}Additional information:
For administration of injections, see manufacturer's labeling.

HYDROCORTISONE SODIUM SUCCINATE FOR INJECTION USP

Note: The dosing and strength of the dosage forms available are expressed in terms of hydrocortisone base (not the sodium succinate salt).

Usual adult and adolescent dose
Corticosteroid
Intramuscular or intravenous, 100 to 500 mg (base); may be repeated every two to six hours, depending upon patient condition and response. {13}

Note: Initial intravenous dosage should be administered over a period of thirty seconds (100-mg dose) to ten minutes (doses 500 mg or higher). {13}
Maintenance dosage (if required) should be no less than 25 mg per day. {13}

Usual pediatric dose
Adrenocortical insufficiency
Intramuscular or intravenous, 0.19 to 0.28 mg (base) per kg of body weight or 10 to 12 mg per square meter of body surface area a day in three divided doses.

Other indications
Intramuscular, 0.67 to 4 mg per kg of body weight or 20 to 120 mg per square meter of body surface area every twelve to twenty-four hours.

1 gram (base) (Rx) [A-Hydrocort (benzyl alcohol 72 mg){67}] [Solu-Cortef (benzyl alcohol 66.9 mg){13}]Packaging and storage:
Store between 15 and 30 °C (59 and 86 °F), {13} unless otherwise specified by manufacturer.Stability:
Reconstituted solution should be used only if it is clear and should be discarded after 3 days. {13}{57}

Caution:
Use of preparations containing benzyl alcohol is not recommended in neonates. A fatal toxic syndrome consisting of metabolic acidosis, central nervous system (CNS) depression, respiratory problems, renal failure, hypotension, and possibly seizures and intracranial hemorrhages has been associated with this use.Additional information:
For preparation and administration of injections, see manufacturer's labeling.

METHYLPREDNISOLONE

Oral Dosage FormsMETHYLPREDNISOLONE TABLETS USPUsual adult and adolescent dose
Corticosteroid
Oral, 4 to 48 mg a day as a single dose or in divided doses. {28}{41}{42}

Multiple sclerosis, acute exacerbations of
Oral, 160 mg a day for one week, followed by 64 mg every other day for one month. {28}{41}

Usual pediatric dose
Adrenocortical insufficiency
Oral, 0.18 mg per kg of body weight or 3.33 mg per square meter of body surface area a day in three divided doses.{91}

Other indications
Oral, 0.42 to 1.67 mg per kg of body weight or 12.5 to 50 mg per square meter of body surface area a day in three or four divided doses.{91}

Note: Bracketed uses in the Dosage Forms section refer to categories of use and/or indications that are not included in U.S. product labeling.METHYLPREDNISOLONE ACETATE INJECTABLE SUSPENSION USP{15}Usual adult and adolescent dose
Corticosteroid
Intra-articular, intralesional, or soft-tissue injection, 4 to 80 mg, repeated at one- to five-week intervals, if necessary. {26}

Intramuscular, 40 to 120 mg, repeated at one-day to two-week intervals, if necessary.

Multiple sclerosis, acute exacerbations of
Intramuscular, 160 mg a day for one week, followed by 64 mg every other day for one month. {26}

Usual pediatric dose
Adrenocortical insufficiency
Intramuscular, 0.12 mg per kg of body weight or 3.33 mg per square meter of body surface area a day (in three divided doses) every third day; or 0.039 to 0.059 mg per kg of body weight or 1.11 to 1.66 mg per square meter of body surface area once a day.{91}

Other indications
Intramuscular, 0.14 to 0.84 mg per kg of body weight or 4.16 to 25 mg per square meter of body surface area every twelve to twenty-four hours.{91}

80 mg per mL (Rx) [Depo-Medrol (benzyl alcohol){26}]Packaging and storage:
Store between 20 and 25 °C (68 and 77 °F), {17} unless otherwise specified by manufacturer. Protect from freezing.Preparation of dosage form:
For preparation and administration of injections, see manufacturer's labeling.Incompatibilities:
It is recommended that this medication not be diluted or mixed with other solutions because of possible physical incompatibility. {26}Auxiliary labeling:
• Shake well.

Caution:
Use of preparations containing benzyl alcohol is not recommended in neonates. A fatal toxic syndrome consisting of metabolic acidosis, central nervous system (CNS) depression, respiratory problems, renal failure, hypotension, and possibly seizures and intracranial hemorrhages has been associated with this use.Additional information:
Do not administer this medication intrathecally or intravenously.

METHYLPREDNISOLONE SODIUM SUCCINATE FOR INJECTION USP

Note: The dosing and strength of the dosage form available is expressed in terms of methylprednisolone base (not the sodium succinate salt).

Colitis, ulcerative
Intravenous, 40 to 120 mg three to seven times a week for two or more weeks. {45}

High-dose (“pulse”) therapy
Intravenous, 30 mg per kg of body weight administered over at least thirty minutes. {18}{43}{45} This dose may be repeated every four to six hours for forty-eight hours. {18}{43}{45}

Multiple sclerosis, acute exacerbations of
Intramuscular or intravenous, 160 mg a day for one week, followed by 64 mg every other day for one month. {18}{43}

[Pneumonia, Pneumocystis carinii, associated with AIDS, adjunctive treatment]1
Intravenous, 30 mg two times a day on days one through five, 30 mg once a day on days six through ten, and 15 mg once a day on days eleven through twenty-one. {68}{70}{71}{77}

[Spinal cord injury, acute ]
Intravenous, 30 mg per kg of body weight administered over fifteen minutes, followed after forty-five minutes by a continuous infusion of 5.4 mg per kg of body weight per hour, for twenty-three hours. {45}{55}{66}

Usual pediatric dose
Adrenocortical insufficiency
Intramuscular, 0.18 mg (base) per kg of body weight or 3.33 mg per square meter of body surface area a day (in three divided doses) every third day; or 0.039 to 0.059 mg per kg of body weight or 1.11 to 1.66 mg per square meter of body surface area once a day.{91}

[High-dose ("pulse") therapy]1
Intravenous, 30 (base) mg/kg (to a maximum of 1 gram) administered over thirty minutes to one hour once a day for three consecutive days.{91}

[Pneumonia, Pneumocystis carinii, associated with AIDS, adjunctive treatment]1
Children up to 14 years of age: Dosage has not been established. {68}{77}

1 gram (base) (Rx) [Solu-Medrol (diluent—benzyl alcohol 66.8 mg){45}]Packaging and storage:
Store between 20 and 25 °C (68 and 77 °F), {18} unless otherwise specified by manufacturer. Protect from light. {18}{45}Preparation of dosage form:
For preparation and administration of injections, see manufacturer's labeling.Stability:
Use reconstituted solution within 48 hours. {45} Do not use if solution is cloudy or contains a precipitate.

Caution:
Use of diluents or preparations containing benzyl alcohol is not recommended in neonates. A fatal toxic syndrome consisting of metabolic acidosis, central nervous system (CNS) depression, respiratory problems, renal failure, hypotension, and possibly seizures and intracranial hemorrhages has been associated with this use.Additional information:
When used intravenously, Methylprednisolone Sodium Succinate for Injection USP should be administered over a period of 1 to several minutes.

PREDNISOLONE

Oral Dosage FormsPREDNISOLONE SYRUP USPUsual adult and adolescent dose
Corticosteroid
Oral, 5 to 60 mg a day as a single dose or in divided doses. {21}

Multiple sclerosis, acute exacerbations of
Oral, 200 mg a day for one week, followed by 80 mg every other day for one month. {19}

Usual adult prescribing limits
250 mg a day.Usual pediatric dose
Adrenocortical insufficiency
Oral, 0.14 mg per kg of body weight or 4 mg per square meter of body surface area a day in three divided doses.

Other indications
Oral, 0.5 to 2 mg per kg of body weight or 15 to 60 mg per square meter of body surface area a day in three or four divided doses.

Usual pediatric dose
Adrenocortical insufficiency
Intramuscular, 0.14 mg per kg of body weight or 4 mg per square meter of body surface area a day (in three divided doses) every third day; or 0.046 to 0.07 mg per kg of body weight or 1.33 to 2 mg per square meter of body surface area once a day.

Other indications
Intramuscular, 0.17 to 1 mg per kg of body weight or 5 to 30 mg per square meter of body surface area every twelve to twenty-four hours.

Usual pediatric dose
Adrenocortical insufficiency
Intramuscular, 0.14 mg (prednisolone phosphate) per kg of body weight or 4 mg per square meter of body surface area a day (in three divided doses) every third day; or 0.046 to 0.07 mg per kg of body weight or 1.33 to 2 mg per square meter of body surface area once a day.

Other indications
Intramuscular, 0.17 to 1 mg per kg of body weight or 5 to 30 mg per square meter of body surface area every twelve to twenty-four hours.

Canada—
Not commercially available.Packaging and storage:
Store below 40 °C (104 °F), preferably between 15 and 30 °C (59 and 86 °F), unless otherwise specified by manufacturer. Protect from light. {57} Protect from freezing.Preparation of dosage form:
For preparation and administration of injections, see manufacturer's labeling.Stability:
This medication is heat-sensitive and should not be autoclaved.

Canada—
Not commercially available.Packaging and storage:
Store below 40 °C (104 °F), preferably between 15 and 30 °C (59 and 86 °F), protected from light, unless otherwise specified by manufacturer. Protect from freezing.Preparation of dosage form:
For preparation and administration of injections, see manufacturer's labeling.Stability:
For concurrent use of a parenteral-local anesthetic, withdraw the required quantity of corticosteroid suspension into a syringe, then add the local anesthetic. Do not introduce the local anesthetic directly into the multiple-dose vial. Also, the mixture should be injected immediately and any unused portion discarded.

This medication is heat-sensitive and should not be autoclaved.Auxiliary labeling:
• Shake well.

Caution:
Use of preparations containing benzyl alcohol is not recommended in neonates. A fatal toxic syndrome consisting of metabolic acidosis, central nervous system (CNS) depression, respiratory problems, renal failure, hypotension, and possibly seizures and intracranial hemorrhages has been associated with this use.Additional information:
Do not administer this medication intravenously.

PREDNISONE

Oral Dosage Forms

Note: Bracketed uses in the Dosage Forms section refer to categories of use and/or indications that are not included in U.S. product labeling.PREDNISONE ORAL SOLUTION USPUsual adult and adolescent dose
Corticosteroid
Oral, 5 to 60 mg a day as a single dose or in divided doses. {46}{47}{48}

Congenital adrenal hyperplasia
Oral, 5 to 10 mg a day as a single dose.

Multiple sclerosis, acute exacerbations of
Oral, 200 mg a day for one week, followed by 80 mg every other day for one month. {48}

[Pneumonia, Pneumocystis carinii, associated with AIDS, adjunctive treatment]1
Oral, 40 mg two times a day on days one through five, 40 mg once a day on days six through ten, and 20 mg once a day on days eleven through twenty-one. {68}{70}{71}{77}

Usual adult prescribing limits
250 mg a day.Usual pediatric dose
Carditis, rheumatic [ or nonrheumatic]1, acute or
Leukemia or
Tumors
Oral, 0.5 mg per kg of body weight or 15 mg per square meter of body surface area four times a day for two to three weeks; then 0.38 mg per kg of body weight or 11.25 mg per square meter of body surface area four times a day for four to six weeks.

Congenital adrenal hyperplasia
Oral, 5 mg per square meter of body surface area a day in two divided doses.

Nephrotic syndrome
Children up to 18 months of age: Dosage has not been established.

Children 18 months to 4 years of age: Oral, initially 7.5 to 10 mg four times a day.

Children 4 to 10 years of age: Oral, initially 15 mg four times a day.

Children 10 years of age or older: Oral, initially 20 mg four times a day.

Tuberculosis (with concurrent antitubercular therapy)
Oral, 0.5 mg per kg of body weight or 15 mg per square meter of body surface area four times a day for two months.

[Pneumonia, Pneumocystis carinii, associated with AIDS, adjunctive treatment]1
Children up to 14 years of age: Dosage has not been established. {68}{77}

Note: Bracketed uses in the Dosage Forms section refer to categories of use and/or indications that are not included in U.S. product labeling.TRIAMCINOLONE TABLETS USPUsual adult and adolescent dose
Allergic disorders
Oral, 8 to 16 mg a day to achieve control within twenty-four to forty-eight hours. {49}

Arthritis, rheumatoid
Initial: Oral, 8 to 16 mg a day for two to seven days. {49}

Other indications
Oral, initially 8 to 20 mg a day in three or four divided doses. When a satisfactory response is obtained, the dose should be reduced by decrements of 2 mg every two to three days until the lowest dose that maintains the desired effect is reached. {49}

Usual pediatric dose
Adrenocortical insufficiency
Oral, 0.12 mg per kg of body weight or 3.3 mg per square meter of body surface area a day as a single dose or in divided doses.

Neoplastic disease
Oral, initially 1 to 2 mg per kg of body weight a day; dosage may then be adjusted based on patient response. {49}

Other indications
Oral, 0.42 to 1.7 mg per kg of body weight or 12.5 to 50 mg per square meter of body surface area a day as a single dose or in divided doses.

Note: Some pediatric patients with neoplastic disease (acute leukemia) may require initial doses as high as 2 mg per kg of body weight per day.

Note: The dosing and strength of the dosage forms available are expressed in terms of triamcinolone base (not the diacetate salt).

Usual adult and adolescent dose
Adrenocortical insufficiency
Oral, 4 to 12 mg (base) a day as a single dose or in divided doses.

Other indications
Oral, 4 to 48 mg a day as a single dose or in divided doses.

Note: After an initial response has been attained, this medication may be administered on an intermittent schedule. An example of this schedule is as follows: three or four days of medication followed by three medication-free days.
In some patients (e.g., those with systemic lupus erythematosus, acute rheumatic carditis, or certain hematologic disorders), initial doses as high as 60 mg per day may be required.

Usual pediatric dose
Adrenocortical insufficiency
Oral, 0.12 mg (base) per kg of body weight or 3.3 mg per square meter of body surface area a day as a single dose or in divided doses.

Other indications
Oral, 0.42 to 1.7 mg per kg of body weight or 12.5 to 50 mg per square meter of body surface area a day as a single dose or in divided doses.

Note: Some pediatric patients with neoplastic disease (acute leukemia) may require initial doses as high as 2 mg per kg of body weight per day.

Caution:
Use of preparations containing benzyl alcohol is not recommended in neonates. A fatal toxic syndrome consisting of metabolic acidosis, central nervous system (CNS) depression, respiratory problems, renal failure, hypotension, and possibly seizures and intracranial hemorrhages has been associated with this use.Additional information:
Do not administer this medication intravenously.

Do not administer the 10-mg-per-mL strength intramuscularly.

Do not administer the 40-mg-per-mL strength intradermally or intralesionally.

Intramuscular, 40 mg once a week. Alternatively, a dose equal to four to seven times the predetermined oral daily dose may be administered as a single injection and repeated at four-day to four-week intervals as required.

Usual pediatric dose
Corticosteroid
Children up to 6 years of age—Use is not recommended.

40 mg per mL (Rx) [Aristocort Forte][Generic]Packaging and storage:
Store between 15 and 30 °C (59 and 86 °F), {52}{53} unless otherwise specified by manufacturer. Protect from freezing. {52}{53}Preparation of dosage form:
For preparation and administration of injections, see manufacturer's labeling.Stability:
Admixtures containing local anesthetics will retain their potency for one full week.Incompatibilities:
This medication should not be mixed with parenteral-local anesthetic formulations containing preservatives such as parabens or phenol because flocculation of the corticosteroid may occur.Auxiliary labeling:
• Shake well.

Caution:
Use of preparations containing benzyl alcohol is not recommended in neonates. A fatal toxic syndrome consisting of metabolic acidosis, central nervous system (CNS) depression, respiratory problems, renal failure, hypotension, and possibly seizures and intracranial hemorrhages has been associated with this use.Additional information:
Do not administer this medication intravenously. {52}{53}

20 mg per mL (Rx) [Aristospan (benzyl alcohol 0.9%){54}]Packaging and storage:
Store between 15 and 30 °C (59 and 86 °F), {24} unless otherwise specified by manufacturer. Protect from freezing. {24}Preparation of dosage form:
For preparation and administration of injections, see manufacturer's labeling.Stability:
Admixtures containing local anesthetics will retain their potency for one full week.Incompatibilities:
This medication should not be mixed with parenteral-local anesthetic formulations containing parabens, phenol, or other such preservatives because flocculation of the corticosteroid may occur.Auxiliary labeling:
• Shake well. {54}

Caution:
Use of preparations containing benzyl alcohol is not recommended in neonates. A fatal toxic syndrome consisting of metabolic acidosis, central nervous system (CNS) depression, respiratory problems, renal failure, hypotension, and possibly seizures and intracranial hemorrhages has been associated with this use.Additional information:
Do not administer this medication intravenously. {54}

The 5-mg-per-mL strength is recommended for intralesional and sublesional injections only.

The 20-mg-per-mL strength is recommended for intra-articular injection only.

NIH-University of California Expert Panel for Corticosteroids as Adjunctive Therapy for Pneumocystis Pneumonia. Consensus statement on the use of corticosteroids as adjunctive therapy for pneumocystis pneumonia in the acquired immunodeficiency syndrome. New Engl J Med 1990 Nov 22; 323(21): 1500-4.

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